Erowid References Database
Colado MI, Granados R, O'Shea E, Esteban B, Green AR.
“The acute effect in rats of 3,4-methylenedioxyethamphetamine (MDEA, 'eve') on body temperature and long term degeneration of 5-HT neurones in brain: a comparison with MDMA ('ecstasy')”.
Pharmacol Toxicol. 1999 Jun;84(6):261-6.
Administration of a single dose of the recreationally used drug 3,4-methylenedioxyethamphetamine (MDEA or 'eve') to Dark Agouti rats resulted in an acute dose-dependent hyperthermic response. The peak effect and duration
of hyperthermia of a dose of MDEA of 35 mg/kg intraperitoneally was similar to a dose of 3,4-methylenedioxymetham-phetamine (MDMA or 'ecstasy') of 15 mg/kg intraperitoneally. Seven days later this dose of MDMA produced a marked
(=50%) loss of 5-HT and its metabolite 5-H1AA in cortex, hippocampus and striatum and a similar loss of [3H]-paroxetine binding in cortex; these losses reflecting the MDMA-induced neurotoxic degeneration of 5-HT nerve endings. In contrast, administration of MDEA (15, 25 or 35 mg/kg), even at the highest dose, produced only a 20%toss in cortex and hippocam-pus and no decrease in striatum. The neurotoxic effect of MDEA was only weakly dose-dependent. Neither MDEA (35 mg/kg) nor MDMA (15 mg/kg) altered striatal dopamine content 7 days later. MDEA appeared to have about half the potency of MDMA in inducing acute hyperthermia and 25% of the potency in inducing degeneration of cerebral 5-HT
neurones. However since higher doses of MDEA (compared to MDMA) are probably necessary to induce mood changing effects, these data do not support any contention that this compound is a 'safer' recreational drug than MDMA in terms
of either acule toxicity or long term neurodegenerafion.
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